Medical Management of Necrotic Dermatitis Syndrome (“Bell Rot”) in a Collection of Jellies
Julianne E. Steers1, BS; Johanna Sherrill1,3, DVM, MS; James Raymond2, DVM, MS, DACVP; Michael Garner2, DVM, DACV
Within a nine-month period, a number of jellies from a mixed-species gallery at the Aquarium of the Pacific in Long Beach, California (USA) presented to the veterinary department with ulcerative lesions of the umbrellar epidermis2,6,7 of the bell, often called “bell rot.” Affected jellies were housed in species-specific exhibits and included West Coast sea nettles (Chrysaora fuscescens), East Coast sea nettles (Chrysaora quinquecirrha), lagoon jellies (Mastigias papua), blubber jellies (Catostylus mosaicus), sanderia jellies (Sanderia malayensis), moon jellies (Aurelia aurita, Aurelia labiata), and white-spotted jellies (Phyllorhiza punctata).
All jellies were kept in re-circulating “kreisel” tanks that had oval shapes, smooth plexiglass walls, and a continuous circular flow. Tanks contained approximately 132–1,325 L of natural sea water conditioned by sand and ozone filtration prior to use within the exhibit gallery. Additional types of filtration varied between individual kreisels and included protein skimmers and bio-towers. The following water quality parameters were checked weekly and were within normal limits: pH >8.10, salinity 31.0–34.5 ppt, alkalinity >2.0 mEq/L, NH3 <0.05 mg/L, NO2 <0.08 mg/L. Water temperature ranged from 12.8–23.9°C according to species requirements. Jellies were fed a variety of diet items, including nauplii (adult and juvenile brine shrimp), moon jelly slurry, bloodworms, small krill, and cyclopeeze (zooplankton derived from copepods). Although water flow was adjusted as needed for optimal circulation, jellies in several exhibit kreisels were routinely observed hitting tank walls or getting trapped in water outflow valves.
Each affected jelly was isolated into a small, round, glass container of tank water for visual examination. Lesions ranged in depth and severity from erosions and ulcers of the peripheral edges and exumbrellar7 surfaces of the bell to full-thickness tears of the subumbrella7 with subsequent internal organ herniation. Jellies with severe “bell rot” and/or herniation were culled and euthanatized by hypothermia at approximately 5°C. Jellies with lesions less than 3 cm in diameter were isolated within hospital tanks for treatment and observations.
Jellies have an extraordinary ability to regenerate epidermal and mesogleal tissue, with a high degree of muscle-cell plasticity.1,3,5-8 Treatment of the bell lesions consisted of sharp excision of necrotic, damaged tissue plus 3–5 mm margins of healthy tissue using Brown-Adson forceps for stabilization and iris scissors for trimming. No jellies exhibited adverse responses to excisional procedures, and thus, no anesthesia was deemed necessary in these cases. Care was taken to keep dissection and trimming techniques as superficial as possible. Invertebrate pain reception should be considered during any procedure that might inflict pain4 and, thus, the use of anesthesia may be advisable for the management of future cases.
After excision of abnormal tissue, jellies were treated with medicated baths (nitrofurazone) (10 mg/L for 1–2 hour, followed by 2 mg/L continuous immersion) until healed or improved, generally 5–7 days. Jellies receiving both tissue removal and antibiotic immersion regained normal appearance of their bell surfaces within 8–12 weeks and could be placed back on exhibit; however, several individuals with permanent superficial scarring of the bell following procedures were culled due to a lack of exhibit quality. Nerve function following excisional therapy and regeneration1,5,8 remained intact based on observed ability of the bell to continue normal propulsion movements.
Bell tissues from several specimens were preserved in 10% neutral buffered formalin for histopathologic evaluation. Biopsies were embedded in paraffin, sectioned at 5.0 µm, and stained with hematoxylin and eosin (H&E) stain. There was multifocal sloughing and loss of epithelium (ulcers) and moderate to marked multifocal coalescing necrosis of the epidermis (ectoderm) covering the exumbrella. The epidermis lining the subumbrella was less severely affected. Necrotic epidermis was covered by cell debris and few degenerate, necrotic hemocytes. In several cases, the necrosis extended deep into the underlying mesoglea with multifocal infiltration by granulated and un-granulated hemocytes. On the exumbrellar surfaces of two of the jellies there were multiple, round, 10–20 µm algal-like organisms with thick, refractile cell walls. These organisms infiltrated into areas of epidermal and mesogleal necrosis. Two different jellies had rod-like to undulating filamentous bacteria infiltrating the areas of epidermal necrosis; however, a sanderia jelly with bell necrosis had neither bacteria nor algal-like organisms evident within its lesions.
We hypothesize that traumatic bell lesions were sustained by jellies as a result of colliding with tank walls, either accidentally or due to undetected, irregular currents within the kreisels. Damaged epithelium supported invasion by opportunistic bacteria and algal-like organisms, further penetration into the mesoglea, and inflammation (hemocytic infiltration) leading to necrosis. In some tanks, the extended stingers (nematocytes) of hydroid colonies7 present on exhibit walls, likely originating from food sources, may have directly contacted and damaged the delicate bell surfaces of affected jellies.
The algal-like organisms associated with moderate to marked epidermal and mesogleal necrosis were more abundant and microscopically different from commensal algae, or zooxanthellae,2,7 naturally found in certain jellies. Possible sources of these algal-like organisms include addition of newly acquired wild-caught jellies without adequate quarantine, contaminated water supplies, equipment, or food sources, and undetected suboptimal water quality leading to overgrowth of opportunistic noncommensal algae. Further evaluation of the algal-like organisms by electron microscopy is underway in order to better determine treatments or management techniques indicated in the prevention of this syndrome.
Efforts should be made to maintain proper husbandry for captive jellies. Ultraviolet filtration, timed lighting cycles, and dilution by water changes may help reduce presence or numbers of potentially pathogenic microorganisms, including algae. The live-food sources should be examined for possible hydroid contamination before adding them to the exhibit. In addition, water flow within jelly tanks must be quite frequently monitored and adjusted to regulate currents and prevent erratic swimming patterns in resident jellies. General guidelines for captive jelly husbandry are available at the website, http://www.jellieszone.com. (VIN editor: link was not accessible as of 3/1/2021.)
To our knowledge, this is the first report documenting multiple cases of necrotic dermatitis associated with algal-like organisms and bacteria in captive jellies. Surgical excision of the affected tissue, followed by topical anti-bacterial therapy, may potentiate healing and improve cosmetic appearance of the bell surfaces. Frequency of necrotic dermatitis syndrome in jellies from this collection prompted re-evaluation of water-flow design in each system in order to prevent contact with tank walls and subsequent damage to delicate epidermal layers.
We thank the husbandry staff at the Aquarium of the Pacific, especially Dr. Sandy Trautwein (curator of invertebrates), Mr. Mark Loos Gelly (husbandry expert), and Ms. Kenna Koons (water quality technician). We are grateful to the Shedd Aquarium library for locating reprints. Special thanks to Dr. Tanja Zabka (University of California Veterinary Pathology program) for pursuing electron microscopy on our behalf.
1. Brockes J. Muscle escapes from a jelly mould. Curr Biol. 1994;4:1030–1032.
2. Brusca RC, Brusca GJ. Invertebrates. Sinauer Associates, Inc. Publishers, Sunderland, Massachusetts. 1990;228–229.
3. Chapman DM. Microanatomy of the bell rim of Aurelia aurita (Cnidaria: Schyphozoa). Can J Zool. 1999;77:34–46.
4. Hackendahl N, Mashima TY. Considerations in aquatic invertebrate euthanasia. In: Proceedings from the American Association Zoo Veterinarians; 2002; Milwaukee, Wisconsin; 324–329.
5. Lin YCJ, Grigoriev NG, Spencer AN. Wound healing in jellyfish striated muscle involves rapid switching between two modes of cell motility and a change in the source of regulatory calcium. Devel Biol. 2000;225:87–100.
6. Megliutsch PA, ed. Invertebrate zoology. 2nd ed. The Radiata. Oxford University Press; 1972;105-127.
7. Ruppert EE, Barnes RD, eds. Invertebrate zoology. 6th ed. Cnidarians and Ctenophores. San Diego, CA: Saunders College Publishing; 1994:95–173.
8. Sparks AK, ed. Invertebrate Pathology: Noncommunicable Diseases, Reaction to Injury and Wound Repair. New York, NY: Academic Press; 1972:32–37.